Unexpected decrease in necrotizing enterocolitis morbidity during the COVID-19 pandemic-A single-centre retrospective study.

Background: The impact of the coronavirus disease 2019 (COVID-19) pandemic on neonatal necrotizing enterocolitis (NEC) is not well characterised. This cross-sectional study evaluated the potential effects of pandemic-related measures on NEC morbidity in premature infants in a neonatal ward during the COVID-19 pandemic. Methods: This was a retrospective study conducted in a tertiary neonatal ward in eastern and central China over 6 consecutive years (2017, 2018, 2019, 2020, 2021 and 2022). The medical records of 189 premature infants with stage II or III NEC were reviewed for clinical manifestations and aetiologies. The data were analysed and compared between the prepandemic period (2017, 2018, and 2019) and the pandemic period (2020, 2021 and 2022). Results: A total of 9,903 infants with gestational age (GA) < 37 weeks were enrolled, including 5,382 in the prepandemic period and 4,521 in the pandemic period. A reduction in stage II or III NEC morbidity was observed in infants with GA < 37 weeks, with an average annual morbidity of 2.29% (123/5,382) (95% CI, 1.89%-2.68%) in the prepandemic period and 1.46% (66/4,521) (95% CI, 1.11%-1.81%) in the pandemic period. NEC morbidity showed resurgent characteristics in 2021. When prepandemic coinfections were excluded, most cases of NEC with bloodstream infections in the prepandemic period were attributable to Gram-negative bacteria (27/32, 84.38%), mainly Klebsiella pneumoniae, while in the pandemic period they were attributable to Gram-positive bacteria (10/18, 55.56%), mainly Staphylococcus aureus. Antimicrobial susceptibility testing revealed that Klebsiella pneumoniae was 100% sensitive to meropenem, imipenem, ciprofloxacin and levofloxacin and 100% resistant to ampicillin. Staphylococcus capitis was 100% sensitive to vancomycin, linezolid, tetracycline, cotrimoxazole and cefoxitin and 100% resistant to penicillin and benzathine. Conclusions: COVID-19 pandemic-related interventions can reduce the morbidity of NEC and change the pathogen spectrum in patients with bloodstream infections. We need to understand the exact factors leading to these changes.

A narrative review of the research status of exosomes in cardiovascular disease.

OBJECTIVE: Cardiovascular diseases (CVDs) are a major health problem worldwide, and medical workers are actively seeking new and effective methods to predict and treat CVDs. Exosomes are secreted by a variety of cells and exist in a variety of body fluids and tissues. Exosomes play an important role in signal transmission between cells and participate in various physiological and pathological activities of the organism. We sought to identify new diagnosis and treatment ideas related to the application of exosomes in CVDs. BACKGROUND: In the cardiovascular system, exosomes are related to endothelial cells, cardiomyocytes, vascular cells, stem cells, and progenitor cells. They can promote angiogenesis, inhibit ventricular remodeling, improve heart function, inhibit local inflammation, and regulate immune responses. They play an important role in the development, injury, and disease of the cardiovascular system. However, as an emerging field, researchers are still trying to fully understand the role of exosomes and their mechanisms in mediating heart repair. METHODS: We searched the China National Knowledge Infrastructure, Wanfang Database, PubMed, and Web of Science databases to find relevant articles. The Chinese and English search terms were "exosomes" and "cardiovascular disease". Ultimately, 96 articles were included in the review. CONCLUSIONS: Exosomes play an important role in the cardiovascular system, and are widely involved in the occurrence and development of CVDs, such as atherosclerosis (AS), acute myocardial infarction (AMI), heart failure (HF), myocardial ischemia-reperfusion (I/R) injury, pulmonary hypertension (PH), and diabetic heart disease. In this review, we summarize research on exosomes in relation to the mechanisms, diagnoses and treatments of CVDs. We also provide new diagnosis and treatment ideas, and promote the clinical application of exosomes.

Identification of lncRNA-mRNA regulatory network associated with isolated systolic hypertension and atherosclerotic cerebral infarction.

BACKGROUND: Increasingly, evidence has shown that long non-coding RNAs (lncRNAs) play an important role in isolated systolic hypertension (ISH). However, a systematic lncRNA-messenger RNA (mRNA) regulatory network is still absent in isolated systolic hypertension and atherosclerotic cerebral infarction patients (ISH & ACI). This research aimed to establish a lncRNA-mRNA co-expression network in patients with ISH & ACI, to probe into the potential functions of lncRNA in such patients. METHODS: Expression profiles of lncRNA and mRNAs were collected and compared, from 8 patients with ISH and 8 patients with ISH & ACI by RNA-seq data. Differentially expressed lncRNAs and mRNAs were screened out via high-throughput sequencing in the plasma of ISH/ACI patients and control ISH patients. Then, a lncRNA-mRNA interaction network was built using the Pearson correlation coefficient by Cytoscape software. The expression levels of the hub genes and lncRNAs were verified by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) in another 10 ISH/ACI patients and 10 control patients. This study was approved by the responsible institutional review board (IRB) and informed consent was provided by participants. RESULTS: A total of 2,768 differentially expressed lncRNAs and 747 differentially expressed mRNAs were identified. We identified two hub genes (CD226 and PARVB) and 11 lncRNAs in the lncRNA-mRNA interaction network. The results of qRT-PCR and cell assay verified that lncRNAs ENST00000590604 and CD226 are highly expressed in patients of ISH & ACI. Further, CD226 was associated with vascular endothelial cells growth and stability through the platelet activation and focal adhesion pathway. CONCLUSIONS: We established a novel mRNA-lncRNA interaction network. The lncRNAs ENST00000590604 and CD226 might be the potential biomarkers of ISH & ACI.

Potential role of endoplasmic reticulum stress is involved in the protection of fish oil on neonatal rats with necrotizing enterocolitis.

Neonatal necrotizing enterocolitis (NEC) is a serious gastrointestinal disease with high death rate in premature infants. Fish oil (FO) and its constituents have been shown to ameliorate intestinal inflammation and mucosal damage. However, the underlying mechanism of action is not known. In the present study, we divided Sprague-Dawley rats into three groups: control group, NEC model group, and FO pre-feeding+NEC model group. Briefly, one week before NEC modeling, in addition to being fed with milk, the FO pre-feeding+NEC modeling group was fed with FO, the NEC group was fed with saline, and the control group was only inserted a gastric-tube for 7 days. Subsequently, histological assay, Western blot, and ELISA were performed. Pretreatment with FO attenuated the NEC symptoms, alleviated intestinal pathological injury, and decreased the expressions of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Furthermore, pretreatment with FO reduced the expressions of endoplasmic reticulum stress (ERS) related proteins, caspase-12, and glucose-regulated protein 78 (GRP78). In addition, intestinal histopathological scores showed a significant positive correlation with intestinal expressions of IL-6, TNF-α, and caspase-12. Collectively, these results indicate that ERS pathway might be involved in the effect of FO in alleviating intestinal mucosal inflammation and injury in rats with NEC.

Suppression of IRE1α Attenuated the Fatty Degeneration in Parenteral Nutrition-Related Liver Disease (PNALD) Cell Model.

AIMS: To model the parenteral nutrition-associated liver disease (PNALD) in rat normal hepatocytes BRL and investigate the role of endoplasmic reticulum stress- (ERS-) related IRE1α signal in the process of PNALD. METHODS: The BRL cells were treated with different concentrations of soybean oil emulsion (SO) to induce hepatocyte fatty degeneration. The PNALD cell disease model was further confirmed by analysis of Oil Red O staining and biochemical parameters. Next, the IRE1α signal in the process of PNALD. α signal in the process of PNALD. α signal in the process of PNALD. α signal in the process of PNALD. RESULTS: The results of Oil Red O staining indicated that the PNALD was successfully established in BRL cells and the CCK-8 data indicated which 0.6% that SO was further applied to the experiment owing to its better induction of PNALD and less toxicity to the cells. Besides, the value of biochemical parameters (TBIL, DBIL, ALT, and AST) was also elevated in the SO group compared with the NG group. After knockdown of IRE1α signal in the process of PNALD. α signal in the process of PNALD. CONCLUSION: IRE1α was induced in PNALD cell model and suppression of IRE1α resulted in reduced steatosis in this cell disease model. Taken together, our data suggested that the IRE1α pathway may be involved in the development of PNALD.α signal in the process of PNALD. α signal in the process of PNALD. α signal in the process of PNALD.

Respiratory Morbidity and Lung Function Analysis During the First 36 Months of Life in Infants With Bronchopulmonary Dysplasia (BPD).

Purpose: To explore the lung function of bronchopulmonary dysplasia (BPD) in premature infants to guide clinical prevention, early diagnosis and treatment. Methods: Thirty infants with BPD at 4-36 months of corrected gestational age were enrolled and divided into mild BPD and moderate and severe BPD groups. Thirty full-term healthy infants, and 30 non-BPD infants at 4-36 months of corrected gestational age were included as controls. Clinical information, including respiratory infections and re-hospitalization, was compared among these groups. Furthermore, lung function analysis was performed in the infants. Results: The upper respiratory tract infection rate and re-hospitalization rate were significantly higher in the infants with BPD than in the non-BPD infants. The tidal volume/kg, proportion of time to reach peak tidal expiratory flow/total expiratory time, tidal volume exhaled at peak tidal expiratory flow/total tidal volume in BPD group were significantly lower in the BPD group than those in non-BPD group. These values gradually decreased as the severity of BPD increased. The respiratory rate (RR) in BPD group was significantly higher than that in non-BPD group. As the severity of the BPD increased, slope of the descending branch of expiration of tidal breathing flow capacity ring (TBFVL) increased. Conclusion: There is a correlation between the severity of BPD and a poor prognosis of respiratory system. TBFVL can directly reflect the characteristics of Tidal Pulmonary Function in children with different degrees of BPD.

Differential Impacts of Soybean and Fish Oils on Hepatocyte Lipid Droplet Accumulation and Endoplasmic Reticulum Stress in Primary Rabbit Hepatocytes.

Parenteral nutrition-associated liver disease (PNALD) is a severe ailment associated with long-term parenteral nutrition. Soybean oil-based lipid emulsions (SOLE) are thought to promote PNALD development, whereas fish oil-based lipid emulsions (FOLE) are thought to protect against PNALD. This study aimed to investigate the effects of SOLE and FOLE on primary rabbit hepatocytes. The results reveal that SOLE caused significant endoplasmic reticulum (ER) and mitochondrial damage, ultimately resulting in lipid droplets accumulation and ER stress. While these deleterious events induce hepatocyte injury, FOLE at high doses cause only minor ER and mitochondrial damage, which has no effect on hepatic function. SOLE also significantly upregulated glucose-regulated protein 94 mRNA and protein expression. These data indicate that SOLE, but not FOLE, damage the ER and mitochondria, resulting in lipid droplets accumulation and ER stress and, finally, hepatocyte injury. This likely contributes to the differential impacts of SOLE and FOLE on PNALD development and progression.